Disconnection of speech-relevant brain areas in persistent developmental stuttering

口吃 断开 心理学 脑功能偏侧化 脑磁图 部分各向异性 听力学 神经科学 白质 言语障碍 磁共振弥散成像 言语感知 发展心理学 医学 磁共振成像 感知 脑电图 法学 放射科 政治学
作者
Martin Sommer,Martin Koch,Walter Paulus,Cornelius Weiller,Christian Büchel
出处
期刊:The Lancet [Elsevier BV]
卷期号:360 (9330): 380-383 被引量:363
标识
DOI:10.1016/s0140-6736(02)09610-1
摘要

Background The neuronal basis of persistent developmental stuttering is unknown. The disorder could be related to a reduced left hemisphere dominance, which functional neuroimaging data suggest might lead to right hemispheric motor and premotor overactivation. Alternatively, the core deficit underlying stuttering might be located in the speech-dominant left hemisphere. Furthermore, magnetoencephalography study results show profound timing disturbances between areas involved in language preparation and execution in the left hemisphere, suggesting that persistent developmental stuttering might be related to impaired neuronal communication, possibly caused by a disruption of white matter fibre tracts. We aimed to establish whether disconnection between speech-related cortical areas was the structural basis of persistent developmental stuttering. Methods We analysed the speech of 15 people with persistent developmental stuttering and 15 closely matched controls for the percentage of syllables stuttered. We used diffusion tensor imaging to assess participants' brain tissue structure, and used voxel-based morphometry and two-sample t test to compare diffusion characteristics between groups. Findings Diffusion characteristics of the group with persistent developmental stuttering and controls differed significantly immediately below the laryngeal and tongue representation in the left sensorimotor cortex (mean difference in fractional anisotropy 0·04 [95% CI 0·03–0·05]). Interpretation Our findings show that persistent developmental stuttering results from disturbed timing of activation in speech-relevant brain areas, and suggest that right hemisphere overactivation merely reflects a compensatory mechanism, analogous to right hemisphere activation in aphasia.
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